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Ussar, S. ; Griffin, N.W.* ; Bezy, O.* ; Fujisaka, S.* ; Vienberg, S.* ; Softic, S.* ; Deng, L.* ; Bry, L.* ; Gordon, J.I.* ; Kahn, C.R.*

Interactions between gut microbiota, host genetics and diet modulate the predisposition to obesity and metabolic syndrome.

Cell Metab. 22, 516-530 (2015)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Obesity, diabetes, and metabolic syndrome result from complex interactions between genetic and environmental factors, including the gut microbiota. To dissect these interactions, we utilized three commonly used inbred strains of mice-obesity/diabetes-prone C57Bl/6J mice, obesity/diabetes-resistant 129S1/SvImJ from Jackson Laboratory, and obesity-prone but diabetes-resistant 129S6/SvEvTac from Taconic-plus three derivative lines generated by breeding these strains in a new, common environment. Analysis of metabolic parameters and gut microbiota in all strains and their environmentally normalized derivatives revealed strong interactions between microbiota, diet, breeding site, and metabolic phenotype. Strain-dependent and strain-independent correlations were found between specific microbiota and phenotypes, some of which could be transferred to germ-free recipient animals by fecal transplantation. Environmental reprogramming of microbiota resulted in 129S6/SvEvTac becoming obesity resistant. Thus, development of obesity/metabolic syndrome is the result of interactions between gut microbiota, host genetics, and diet. In permissive genetic backgrounds, environmental reprograming of microbiota can ameliorate development of metabolic syndrome.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Intestinal Microbiota; Insulin Sensitivity; Wide Association; Systems Biology; Mice; Disease; Individuals; Homeostasis; Metagenome; Resistance
ISSN (print) / ISBN 1550-4131
e-ISSN 1932-7420
Journal Cell Metabolism
Quellenangaben Volume: 22, Issue: 3, Pages: 516-530 Article Number: , Supplement: ,
Publisher Elsevier
Publishing Place Cambridge
Non-patent literature Publications
Reviewing status Peer reviewed